An obstacle to treating certain viral infections, such as Human Immunodeficiency Virus (HIV), is the existence of a pool of infected resting memory CD4+ T cells (Chun T W et al., Nat Med 1: 1284-90, 1995; Chun T W et al., Nature 387:183-88, 1997). Cells in this resting state do not produce virus and thus neither die by viral cytopathic mechanisms nor are they effectively targeted by the immune system. Upon cessation of antiviral therapy, these cells are thought to re-seed systemic infection, likely as a result of sporadic activation. The longevity of resting memory CD4+ T cells, with a half-life of 44 months, renders this ‘latent reservoir’ an obstinate barrier to eradication.